Participation of Nrf2-ARE Signaling in Curcumin Inhibition of Amyloid-β-induced Cellular Oxidative Stress and Cell Apoptosis
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Abstract:
This study investigated the protective effects of curcumin on cellular oxidative damage and cell apoptosis induced by amyloid-β (Aβ) in human neuroblastoma SH-SY5Y cells and discussed the role of the Nrf2-antioxidant response element (ARE) pathway in this protective effect. Cells were treated with 10 μM Aβ1-40 at 37 ℃ for 24 h with or without curcumin pre-treatment. The changes in morphology were observed under the microscope, and the MTT colorimetric assay was used to assess cell viability. Lactate dehydrogenase (LDH) in the culture medium was determined to evaluate cell membrane damage. The relative levels of H2O2 in the culture medium and intracellular reactive oxygen species (ROS) were assessed. In addition, the protein expressions of Nrf2 and HO-1 were detected by western blot analysis. Compared with the vehicle-only control group, cell bodies in the Aβ-damaged group became rounded, with fewer and shorter protuberances. Cell viability decreased, and the level of released LDH increased, while the oxidative stress level was significantly elevated. Compared with the Aβ-damaged group, curcumin treatment promoted cell growth and the protuberances became longer; cell viability increased while released LDH decreased, and the level of oxidative stress also decreased significantly. Notably, curcumin promoted Nrf2 expression and attenuated Aβ-induced up-regulation of phosphorylated Nrf2 at Ser-40 as well as HO-1 expression. Curcumin attenuated cellular oxidative damage and cell apoptosis induced by Aβ, which might be linked to the regulation of the Nrf2-ARE pathway by curcumin.
